In addition to etiological components characterizing AUDs, i.e. a certain genetic variant that predisposes an individual to excessive alcohol consumption, there are also more pathophysiological components. Pathophysiological effects include the cellular, molecular and synaptic phenotypes produced upon acute alcohol administration. There is compelling evidence to suggest that alcohol primarily targets the synapse (Lovinger & Roberto, 2013). In fact, excitatory N-methyl-D-aspartate (NMDA) and inhibitory gamma aminobutyric acid type-A (GABAA) ligand-gated ionotropic receptors are two of alcohol’s main targets. Furthermore, alcohol has been shown to act as a potent epigenetic modulator impacting cellular metabolism and differentiation. Specifically, neuroinflammation and oxidative stress (damage) of the mitochondria and cellular proteins are believed to add to the progression of neurological disorders that are caused by alcohol abuse (Alfonso-Loeches, Ureña-Peralta, Morillo-Bargues, Oliver-De La Cruz, & Guerri, 2014; De Filippis et al., 2016). Numerous studies using both in vitro and in vivo animal models, as well as postmortem human brain tissue have laid the groundwork for most of the theories explaining the molecular underpinnings of AUDs. However, animal models do not completely mimic disease initiation and progression
